Chapter Notes: Cardiovascular System - 1

Table of Contents
1. Overview of the Heart
2. Understanding Heart Failure
3. Rheumatic Fever and Rheumatic Heart Disease (RHD)
4. Infective Endocarditis (IE)
5. Marantic Endocarditis/ Non-Bacterial Thrombotic Endocarditis (NBTE)
6. Libman-Sacks Endocarditis (SLE)
7. Overview of Barlow Syndrome
8. Ischemic Heart Disease
9. Cardiac Tumors
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Overview of the Heart

The human heart is a muscular organ that plays a crucial role in maintaining blood circulation throughout the body. It supplies oxygen and nutrients to various organs and tissues. The heart consists of four chambers: the left and right atria (upper chambers) and the left and right ventricles (lower chambers). The left ventricle is responsible for pumping oxygenated blood to the body, while the right ventricle pumps deoxygenated blood to the lungs for oxygenation.

• The left ventricle has a much thicker muscular wall compared to the right ventricle because it needs to generate higher pressure to pump blood throughout the body.
• On average, the heart pumps about 5 litres of blood every minute, although this can vary depending on factors such as physical activity and overall health.

Coronary Arteries

• Left Coronary Artery. This artery branches into two main arteries:
• Left Anterior Descending (LAD) Artery. Supplies blood to the:
• Apex of the heart
• Anterior two-thirds of the interventricular septum (the wall separating the left and right ventricles)
• Anterior wall of the left ventricle
• Left Circumflex (LCX) Artery. Primarily supplies blood to the lateral wall of the left ventricle.
• Right Coronary Artery (RCA). Supplies blood to the:
• Entire right ventricular free wall
• Posterobasal wall of the left ventricle
• Posterior one-third of the interventricular septum.

Collateral Perfusion

• Endocardium. Among the three layers of the heart-the pericardium (outer layer), myocardium (middle layer), and endocardium (inner layer)-the endocardium has the least collateral perfusion.
• Risk of Ischaemia. This means that during conditions such as hypotension (low blood pressure) or shock, there is a higher risk of subendocardial ischaemia (reduced blood flow to the inner layer of the heart).
• Coronary Dominance. The coronary artery that supplies the posterior one-third of the ventricular septum through the posterior descending artery is termed dominant. In about 70-80% of people, this artery comes from the RCA, indicating right dominant circulation.

Myocardium and Cardiac Muscle

• The myocardium, also known as cardiac muscle, is made up of cardiac myocytes (heart muscle cells). Unlike other types of muscle cells, cardiac myocytes do not divide or grow in response to stress.
• The only change that can occur in cardiac muscle in response to stress is hypertrophy, which is an increase in the size of the muscle cells. There are two types of hypertrophy:
• Concentric Hypertrophy. This type is related to pressure overload, where the heart has to pump against increased resistance, such as in hypertension.
• Volume Overload Hypertrophy. This type is associated with dilatation, where the heart chambers enlarge due to increased blood volume, such as in heart failure.

Cardiac Output

• Stroke Volume. The volume of blood pumped by the heart in one beat is called stroke volume, which is approximately 70 ml.
• Ejection Fraction. The normal ejection fraction, which is the percentage of blood pumped out of the heart with each beat, is around 65%.

Energy Source for Cardiac Myocytes

• Fatty Acids. The primary source of energy for cardiac myocytes is fatty acids. These are broken down in the mitochondria of the cells to produce adenosine triphosphate (ATP), which is used for various cellular functions, including muscle contraction.

Heart's Pacemaker and Gatekeeper

• SA Node. The sinoatrial (SA) node acts as the heart's natural pacemaker. It is located in the right atrium and generates electrical impulses that initiate each heartbeat. These impulses cause the atria to contract and pump blood into the ventricles.
• AV Node. The atrioventricular (AV) node functions as the gatekeeper of the heart. It is located between the atria and ventricles and receives the electrical impulses from the SA node. The AV node delays these impulses for a fraction of a second, allowing the ventricles to fill with blood before they contract and pump blood out of the heart.

Understanding Heart Failure

Heart failure is when the heart struggles to pump blood as needed, either effectively or under high pressure. It can be divided into two main types:

• Systolic failure. The heart's contraction ability is weakened, often due to conditions like ischemic heart disease, pressure overload, or dilated cardiomyopathy.
• Diastolic failure. The heart has difficulty relaxing, commonly seen in conditions like constrictive pericarditis or myocardial fibrosis.

Left Ventricular Failure (LvF)

Causes

The primary causes of left ventricular failure include:

• Ischemic heart disease
• Hypertension
• Aortic or mitral valve diseases
• Non-ischemic myocardial disease

Key Features

• Thickening and scarring of the heart muscle, leading to enlargement of the atria.
• Enlarged atria increase the risk of atrial fibrillation, which can result in blood clots and strokes.

Affected Organs

Lungs

• Increased pressure in the pulmonary veins causes pulmonary edema, resulting in fluid buildup in the lungs.
• This fluid interferes with gas exchange, leading to symptoms such as:
  • Dyspnea (shortness of breath)
  • Orthopnea (difficulty breathing when lying down)
  • Paroxysmal nocturnal dyspnea (sudden nighttime breathlessness)
• Chest X-rays may reveal Kerley B lines due to fluid in the lung tissue.

Kidneys

• Initially, reduced blood flow to the kidneys triggers the renin-angiotensin-aldosterone system.
• In advanced stages, persistent low blood flow can lead to prerenal azotemia.

Brain

• The brain may suffer from hypoxic-ischemic encephalopathy due to inadequate blood flow and oxygen.

Right-sided Heart Failure

Right-sided heart failure often stems from left ventricular failure but can also occur independently in cases of severe chronic pulmonary hypertension, a condition known as cor pulmonale.

Key Features

• Liver. Congestive hepatomegaly may occur. In cases associated with left ventricular failure, centrilobular necrosis can lead to cardiac cirrhosis.
• Spleen. Congestive splenomegaly may be observed.
• Azotemia. Congestion can lead to severe azotemia, more pronounced in right-sided heart failure compared to left-sided failure.
• Other Manifestations :
• Pleural effusion
• Pericardial effusion
• Ascites
• Peripheral Edema. The primary sign of right-sided heart failure is peripheral edema, especially in the legs and feet.
• Anasarca refers to severe generalized swelling seen in heart failure.

Rheumatic Fever and Rheumatic Heart Disease (RHD)

Overview: Rheumatic fever is an inflammatory disease that can affect various systems in the body. It typically occurs a few weeks after a throat infection caused by group A β-hemolytic streptococci. This condition is not contagious and primarily affects children between the ages of 5 to 15. However, only about 3% of those with group A streptococcal throat infections develop rheumatic fever.

Mechanism: Rheumatic fever is an example of a type II hypersensitivity reaction. In this condition, antibodies produced against the 'M' protein of certain streptococcal strains mistakenly attack the body's own tissues, including the heart, joints, and other organs. This occurs due to a phenomenon known as molecular mimicry, where the antibodies confuse the body's own tissues for the bacteria.

WHO Criteria for Diagnosis of Rheumatic Fever and Rheumatic Heart Disease
Major Manifestations:

• Joint Involvement (Polyarthritis): Inflammation of multiple joints.
• Nodules (Subcutaneous): Painless lumps under the skin, often found on the elbows, shins, and back of the head.
• Erythema Marginatum:. distinctive red rash that typically appears on the trunk and limbs, sparing the face.
• Sydenham's Chorea: Involuntary movements and emotional instability, often occurring as a late manifestation of rheumatic fever.
• Carditis: Inflammation of the heart, affecting all three layers of the heart (pancarditis), with common involvement of the mitral valve.

Minor Manifestations:

• Clinical: Fever, polyarthralgia (pain in multiple joints).
• Laboratory: Increased erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP).
• ECG: Prolonged PR interval.

Supporting Evidence of Preceding Streptococcal Infection:

• Elevated or rising antistreptolysin O (ASO) or other antibody titers.
• Positive throat culture for group A streptococcus.
• Rapid antigen test for group A streptococcus.

Note:

• To diagnose the first episode of rheumatic fever, either two major manifestations or one major and two minor manifestations, along with evidence of a recent group A streptococcal infection, are required.
• The 1992 revised Jones criteria do not consider elevated total leukocyte count (TLC) as a minor laboratory manifestation and do not recognize recent scarlet fever as supporting evidence of a recent streptococcal infection.

Salient Features Of THE Major Criteria

• Pancarditis: Involvement of all three layers of the heart - pericardium, myocardium, and endocardium.
• Pericarditis: Characterized by a fibrinous or serofibrinous exudate, often described as "bread and butter" pericarditis.
• Valvular Involvement: Common in rheumatic heart disease, particularly affecting the mitral valve. Mitral regurgitation is typical in acute cases, while mitral stenosis is more common in chronic cases.
• Migratory Polyarthritis: Affects large joints, more frequently seen in adults. The arthritis is migratory and self-resolving, without causing lasting joint damage. This is the most commonly observed symptom, and joint pain responds well to salicylates like aspirin.
• Subcutaneous Nodules: Painless lumps located under the skin, usually on the outer surfaces of the elbows, shins, and back of the head.
• Erythema Marginatum:. non-scarring red macular rash, more apparent in individuals with fair skin, sparing the face.
• Sydenham's Chorea:. late-onset symptom characterized by involuntary movements and emotional instability.

Microscopic Features:

• Aschoff's Bodies: Key feature in rheumatic heart disease, consisting of swollen collagen surrounded by T-lymphocytes, plasma cells, and Anitschkow cells (macrophages specific to rheumatic fever). Anitschkow cells, also known as "caterpillar cells," have abundant cytoplasm and round to oval nuclei with wavy ribbon-like chromatin.
• Myocardial Involvement: Aschoff's bodies are found in the myocardium near blood vessels.
• Endocardial Involvement: Leads to fibrinoid necrosis in valve cusps or along tendinous cords, with small growths called verrucae along closure lines. Mitral regurgitation can cause irregular thickening of the left atrial wall, known as MacCallum plaques.

Chronic Rheumatic Heart Disease: Characterized by organized acute inflammation and subsequent scarring. Valves show thickening, fusion at commissures, and shortening of tendinous cords. Mitral stenosis, often referred to as "fish-mouth" or "button-hole" stenosis, may lead to atrial fibrillation and thromboembolic complications.

Infective Endocarditis (IE)

Endocarditis occurs when microbes invade the heart valves and the inner lining of the heart, leading to the formation of large, fragile masses composed of blood clots and pathogens. This invasion can cause damage to the heart tissue.

Types of Endocarditis

• Acute endocarditis
• Subacute endocarditis

Acute endocarditis

• Involves a rapid infection on a previously normal valve.
• Caused by highly virulent organisms.
• Can lead to death within days to weeks.
• Most commonly caused by Staphylococcus aureus.

Subacute endocarditis

• Involves a slower infection on a previously damaged valve.
• Caused by low virulence organisms.
• Patients often recover after antibiotic treatment.
• Most commonly caused by viridans group streptococci.

Important Microbiology Link!

• Organisms in infective endocarditis :
• Staphylococcus aureus. Common in intravenous drug users.
• Staphylococcus epidermidis. Found in patients with prosthetic or artificial valves.
• Staphylococcus viridans. Associated with patients having previously damaged valves.
• Staphylococcus mutans. Linked to patients who have had recent tooth extractions.
• Other organisms include enterococci and the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella).

Morphology

• The large, fragile vegetations contain fibrin, bacteria, and inflammatory cells.
• These vegetations are primarily found on the valve cusps and can extend onto the chordae.
• The aortic valve and mitral valve are the most commonly infected.
• In intravenous drug users, the right side of the heart is often affected.
• When vegetations erode into the heart muscle, they can create an abscess known as a ring abscess.
• This condition can lead to systemic embolization and septic infarcts.

Clinical Features

• Fever is the most consistent sign of infective endocarditis.
• Other symptoms include:
• Weight loss
• Flu-like symptoms
• Cardiac murmur
• Systemic emboli
• Roth spots (due to retinal emboli)
• Osler nodes (painful nodules on fingers and toes)
• Janeway lesions (painless red spots on palms and soles)

The disease is diagnosed using the Duke's criteria.

Complications

Cardiac complications include:

• Valvular insufficiency or stenosis
• Myocardial ring abscess
• Suppurative pericarditis
• Valvular dehiscence

Embolic complications can affect:

• Left-sided lesions - Brain, spleen, kidney
• Right-sided lesions - Lung infarct, lung abscess

Renal complications can include:

• Embolic infarct
• Focal (more common) or diffuse glomerulonephritis (less common)

Marantic Endocarditis/ Non-Bacterial Thrombotic Endocarditis (NBTE)

• Marantic endocarditis, also known as non-bacterial thrombotic endocarditis (NBTE), is a condition that affects patients with severe illnesses such as cancer (e.g., pancreatic cancer and acute promyelocytic leukemia) and conditions that increase blood clotting, like disseminated intravascular coagulation (DIC).
• In this type of endocarditis, vegetations on the heart valves are sterile, meaning they do not contain any microorganisms. These vegetations typically form along the line of closure of the valve leaflets and can be either single or multiple.

Libman-Sacks Endocarditis (SLE)

Libman-Sacks endocarditis is a type of endocarditis associated with systemic lupus erythematosus (SLE). In this condition, the vegetations are small to medium-sized, sterile, granular, and pink in appearance. They can be found on one or both sides of the valve leaflets, particularly affecting the mitral and tricuspid valves.

Both the mitral and tricuspid valves exhibit fibrinoid necrosis in Libman-Sacks endocarditis.

Here's a summary of the key features of vegetations in different types of endocarditis:

• Non-Bacterial Thrombotic (Marantic Endocarditis)
• Libman-Sack's Endocarditis
• Size: Small, warty Size: Medium-sized (small)
• Texture: Firm Texture: Flat, verrucous
• Texture: Friable Shape: Irregular
• Location: Along lines of closure Location: On surface of cusps (both surfaces may be involved, but the undersurface is more likely to be affected; less commonly, mural endocardium is involved)
• Location: In pockets of valves Location: Vegetations on the valve cusps, less often on mural endocardium
• Sterility: Sterile (no organism) Sterility: Non-sterile (bacteria)
• Embolization: Uncommon Embolization: Common
• Embolization: Very common (maximum chances)
• Causes: In rheumatic heart disease Causes: In cancers (e.g., acute myeloid leukemia, M3 subtype, pancreatic cancer), deep vein thrombosis, Trousseau syndrome Causes: In SLE Causes: In infective endocarditis

The most frequent causes of functional valvular lesions are:

• Aortic stenosis: Caused by calcification of anatomically normal and congenitally bicuspid aortic valves.
• Aortic regurgitation: Results from dilation of the ascending aorta due to hypertension and aging.
• Mitral stenosis: Primarily due to rheumatic heart disease.
• Mitral regurgitation: Often due to myxomatous degeneration, commonly known as mitral valve prolapse.

Overview of Barlow Syndrome

• Sudden cardiac death is frequently triggered by ventricular fibrillation.
• In an ECG, subendocardial ischemia is indicated by ST segment depression.
• This syndrome is more prevalent in females.

Mitral Valve Prolapse

• In valvular abnormalities associated with this condition, one or both mitral leaflets are "floppy" and may prolapse, meaning they bulge back into the left atrium during systole. This leads to a characteristic mid-systolic click.
• Most patients with mitral valve prolapse are typically asymptomatic.
• The condition is often discovered during a routine examination when a midsystolic click is detected.
• In cases where mitral regurgitation is present, there may be a late systolic or sometimes holosystolic murmur.
• Some patients may experience chest pain similar to angina, along with dyspnea, fatigue, or psychological symptoms such as depression, anxiety, and personality disorders.

Microscopic Changes in Myxomatous Degeneration

• The primary microscopic change in myxomatous degeneration is the intercordal ballooning or hooding of parts or all of the mitral leaflets.
• The affected leaflets are often enlarged, redundant, thick, and have a rubbery texture.
• The tendinous cords may be elongated, thin, and in some cases, ruptured.
• Annular dilation is a common feature in this condition, which is rare in other causes of mitral insufficiency.

Diagnosis and Risk Factors

• Mitral valve prolapse is diagnosed through echocardiography.
• The risk of complications such as infective endocarditis, mitral insufficiency, stroke or other systemic infarcts, and arrhythmias is higher in men, older patients, and those with arrhythmias or some degree of mitral regurgitation.
• The presence of holosystolic murmurs and left-sided chamber enlargement indicates a higher risk of these complications.

Ischemic Heart Disease

Ischemic heart disease occurs when there is not enough oxygen-rich blood reaching the heart, which is crucial for its function. This condition is primarily caused by the narrowing of coronary arteries due to a process called atherosclerosis, where fatty deposits build up on the artery walls.

Types of Ischemic Heart Disease

Sudden Cardiac Death

• Definition: Sudden cardiac death is defined as death occurring within 1 hour of the first symptoms appearing.
• Cause: It is most often caused by ventricular fibrillation, a life-threatening heart rhythm that results in rapid, inadequate heartbeat.
• Mechanism: When coronary vessels are blocked, it leads to ischemia (insufficient blood supply), prompting the body to compensate by widening blood vessels to increase blood flow to the heart.
• Degree of Blockage: If the blockage in the arteries is 75% or more, ischemic symptoms can occur during exercise. If the blockage exceeds 90%, symptoms can manifest even at rest.
• Trigger: This condition is often triggered by the rupture or ulceration of a plaque in the arteries.

Stable Angina

• Definition: Stable angina occurs when the heart's demand for oxygen exceeds the supply, typically due to significant blockage of the coronary artery.
• Blockage Severity: This usually happens when the coronary artery is blocked by more than 75%.
• Symptoms: It is characterized by chest pain or discomfort during physical activity, which subsides with rest or medication such as nitrates.
• Plaque Stability: There is no disruption of plaques or blood clots involved in stable angina.
• ECG Changes: Electrocardiogram (ECG) changes may show ST segment depression and T wave inversion, indicating subendocardial ischemia of the left ventricle.

Prinzmetal or Variant Angina

• Nature: Prinzmetal or variant angina is episodic and occurs due to a spasm in the coronary artery.
• Symptoms: This type of angina can cause chest pain even at rest.
• ECG Findings: It is identifiable by ST segment elevation on the ECG, which indicates transmural ischemia (full thickness of the heart wall) due to the spasm.

Unstable or Crescendo Angina

• Cause: Unstable or crescendo angina occurs due to the disruption of atherosclerotic plaques in the coronary arteries.
• Blood Clots and Spasms: It may involve partial blood clots or spasms in the arteries.
• Symptoms: The pain associated with unstable angina becomes more frequent, lasts longer, and is triggered by less exertion than before.

Myocardial Infarction (MI)

• Subendocardial MI: This type of myocardial infarction involves necrosis (tissue death) affecting only a third of the ventricular wall. It occurs due to incomplete blockage of the coronary artery.
• Transmural MI: In this more severe form, necrosis involves the entire thickness of the ventricular wall. This is typically caused by severe coronary atherosclerosis (narrowing of the arteries) and acute plaque rupture accompanied by a blood clot.

Pathogenesis of MI

• Changes in an atheromatous plaque, such as hemorrhage or rupture, lead to the exposure of collagen.
• This exposure causes platelets to aggregate, triggering vasospasm and activating the clotting pathway.
• These processes result in the complete blockage of the coronary vessel, leading to myocardial infarction.

Myocardial Response to Infarction

• Time: The response of the myocardium (heart muscle) to infarction can be measured over time, starting from the cessation of aerobic respiration and the onset of ATP depletion.
• Seconds: Within seconds of the infarction, there is a loss of contractility in the heart muscle.
• 2 Minutes: ATP levels are reduced to 50% of normal.
• 10 Minutes: ATP levels drop to 10% of normal.
• 40 Minutes: Irreversible cell injury occurs at this stage.
• 20-40 Minutes: Microvascular injury may occur during this time frame.
• More than 1 Hour: Severe damage to the myocardium is observed.

Evolution of Morphological Changes in MI

• Gross Changes:
• 0-30 minutes: Reversible injury, no visible changes.
• 30 minutes to 4 hours: Irreversible injury, changes begin to occur.
• 4-12 hours: Early signs of damage, such as dark mottling.
• 12-24 hours: Ongoing damage, inflammation begins to set in.

ECG Changes: In cases of transmural ischemia, ST segment elevation is observed on the ECG, indicating the severity of the condition.

Differentiating Angina from Myocardial Infarction

• The primary distinction between angina and myocardial infarction (MI) lies in the elevation of cardiac enzymes.
• In MI, cardiac enzymes are elevated, indicating heart muscle damage.
• In some cases of angina, cardiac enzymes may be elevated, but this is not typical.
• Neutrophil and Macrophage Infiltration: Neutrophils infiltrate the damaged area between 48-72 hours after MI.
• After this period, macrophages take over the cleanup process, removing dead cells.

MI in Diabetic Patients: MI is a leading cause of death in patients with diabetes. These patients may experience 'silent' MIs, where symptoms are not apparent.

Sequence of Elevated Enzymes after MI

• Myoglobin: This enzyme is the first to rise after MI, indicating muscle damage.
• Troponin: This enzyme is the most sensitive and specific marker for MI.
• CK-MB: This enzyme is best for diagnosing reinfarction, indicating a new episode of heart muscle damage.
• 1-3 days: The centre of the infarcted area becomes yellow-tan as necrosis progresses.
• 3-7 days: Hyperaemic borders (increased blood flow) are observed, and disintegration of tissue begins.
• 7-10 days: Granulation tissue starts to form in the infarcted area.
• 10-14 days: Established granulation tissue and collagen deposition occur in the infarcted area.
• 2-8 weeks: Scar formation progresses from the border of the infarct to the core.
• More than 2 months: Complete scarring with dense collagen is achieved in the infarcted area.

Diagnosis of Infarcts

Triphenyl tetrazolium chloride (TTC) is a dye used to diagnose infarcts in cardiac tissue when they are less than 12 hours old. This dye reacts with the LDH enzyme, which is present only in living cardiac fibers. When TTC comes into contact with living tissue, it produces a brick-red color, indicating the presence of viable cells. In contrast, tissue that has undergone infarction appears as an unstained pale zone, indicating cell death.

Microscopic Features of Reperfusion

• In cases of infarction modified by reperfusion, the distinctive microscopic feature observed is necrosis accompanied by the presence of contraction bands.
• In myocytes that have been irreversibly injured, there is an increase in calcium ions, leading to hypercontraction of the sarcomeres. This hypercontraction is a typical response to irreversible cellular injury.

Diagnosis of Myocardial Infarction

Myocardial Infarction (MI) should be suspected in patients presenting with:

• Intense chest pain
• Rapid and weak pulse
• Profuse sweating
• Difficulty breathing (dyspnea)
• Swelling (edema)

Among these symptoms, a rapid pulse is often the first indicator, while dyspnea is a crucial sign of acute MI. An electrocardiogram (ECG) during acute MI typically shows ST segment elevation. In contrast, the presence of a 'Q' wave on the ECG signifies a previous (old) MI.

Laboratory Investigations

Laboratory tests for MI can reveal both non-specific and specific markers of the condition.

Non-specific markers include:

• Elevated Erythrocyte Sedimentation Rate (ESR)
• Leukocytosis (increased white blood cell count)
• Raised levels of C-reactive protein (CRP)

Specific markers for myocardial injury include:

• Troponin T and I (TnT, TnI)
• Initial rise: 2-4 hours after injury
• Peak levels: around 48 hours
• Aspartate Aminotransferase (AST/SGOT)
• Initial rise: approximately 12 hours post-injury
• Peak levels: 4-5 days after injury
• Return to baseline: usually within 2 weeks

Cardiac Enzymes

• Troponin T and Troponin I
  • These proteins play a crucial role in the contraction of heart and skeletal muscles.
  • They are highly specific for diagnosing myocardial infarction (MI).
  • Troponin I is more significant than Troponin T (think of "I" for "Important").
  • If a patient experiences a reinfarction within one week, these enzymes cannot be used for diagnosis because their levels remain elevated for a long time after the initial event.
  • In such cases, it is better to use enzymes that increase for a shorter period.
• Creatine kinase (CK)
  • This enzyme is an alternative to measuring troponin levels.
  • There are three isoforms of CK:
    • CK-MM. Found in skeletal muscle and the heart.
    • CK-MB. Found in the myocardium (heart muscle) and a small amount in skeletal muscle.
    • CK-BB. Found in the brain, lung, and other tissues.
  • Elevation of the CK-MB isoform indicates myocardial infarction (MI).
  • If there is no rise in CK-MB levels within the first two days, it rules out MI.
  • CK-MB is commonly used for diagnosing reinfarction due to its rapid increase and decrease in serum levels (limited detection window).
  • It is also the earliest enzyme to rise after MI.
• Normally, serum LDH2 is higher than LDH1, but during MI, LDH1 levels surpass LDH2 levels.
• This change is referred to as the "flipping of the LDH ratio."

Complications of Myocardial Infarction

• Contractile Dysfunction: This can lead to cardiogenic shock, a condition where the heart suddenly can't pump enough blood to meet the body's needs.
• Arrhythmias:
  • Ventricular Fibrillation: This is the most common type of arrhythmia in the first hour after a heart attack.
  • Supraventricular Tachycardia: This type of arrhythmia becomes more common after the first hour of myocardial infarction.
• Cardiac Rupture Syndrome:
  • Ventricular Free Wall Rupture: This is the most common type of cardiac rupture, leading to a condition called cardiac tamponade.
  • Common Site: The anterolateral wall at midventricular level is the most common site for rupture.
  • Timing: Rupture typically occurs 3 to 7 days after a myocardial infarction due to weakening of the tissue.
  • Ventricular Septum Rupture: This can create a left-to-right shunt, altering blood flow in the heart.
  • Papillary Muscle Rupture: This can lead to mitral regurgitation, where blood leaks backward through the mitral valve.
• Pericarditis:
  • Definition: Pericarditis is an inflammation of the pericardium, the outer layer of the heart, and is associated with myocardial damage.
  • Also Known As: It is sometimes referred to as Dressler syndrome or post-myocardial infarction syndrome.
  • Timing: This autoimmune reaction typically occurs 2 to 3 weeks after a transmural myocardial infarction but can occur as early as 48 hours post-infarction.
  • Symptoms: Pericarditis is associated with pleural effusion, pleuritic chest pain, and pericardial effusion.
• Right Ventricular Infarction: This is a complication where the right ventricle of the heart also suffers damage during a myocardial infarction.
• Ventricular Aneurysm: This condition can lead to thromboembolism, where blood clots travel to different parts of the body.
• Papillary Muscle Dysfunction: This condition results in mitral regurgitation following a myocardial infarction.
• Dressler Syndrome Treatment: Dressler syndrome is typically treated with non-steroidal anti-inflammatory drugs (NSAIDs), and in some cases, steroids may be used.
• Left Ventricular Rupture: This is a serious complication of acute myocardial infarction, usually occurring 4 to 7 days after the infarction when the necrotic area has the least tensile strength and the repair process is just beginning.

Cardiac Tumors

Myxoma

• Myxomas are the most prevalent type of primary heart tumor in adults.
• These tumors can form in any chamber of the heart, but approximately 90% are found in the atria, with a left-to-right ratio of about 4:1.
• Symptoms primarily result from blockages resembling a "ball-valve," the potential for blood clots, or general symptoms like fever and fatigue, often linked to interleukin-6.
• Around 10% of individuals with myxoma have a genetic condition called Carney syndrome, which is inherited in an autosomal dominant fashion.
• Carney syndrome is characterized by multiple myxomas in the heart and other parts of the body (such as the skin), skin pigmentation changes, and endocrine disorders.
• The genetic basis of this syndrome is a mutation in the PRKAR1 gene on chromosome 17, which functions as a tumor suppressor.
• Myxomas are usually solitary and most commonly arise from the fossa ovalis in the atrial septum.
• Histologically, myxomas are composed of stellate or rounded cells, endothelial cells, smooth muscle cells, and undifferentiated cells within a rich mucopolysaccharide matrix, all covered by endothelium.

Rhabdomyoma

• Rhabdomyomas are the most prevalent benign heart tumors in infants and children.
• These tumors are more accurately described as malformations (hamartomas) rather than true tumors.
• Cardiac rhabdomyomas are associated with tuberous sclerosis, which results from defects in the TSC1 or TSC2 tumor suppressor genes.
• The TSC proteins promote cell growth and contribute to the overgrowth of muscle cells.
• Rhabdomyomas typically present as small, grey-white nodules protruding into the heart's chambers.
• Histologically, they consist of large, rounded or polygonal cells packed with glycogen-rich vacuoles, with strands of cytoplasm extending to a centrally located nucleus, giving rise to the characteristic "spider cells."
• The most prevalent heart tumor overall is secondary or metastatic in nature.
• The most common primary heart tumor in adults is the myxoma.
• The most frequent heart tumor in children is the rhabdomyoma.